Top Spinal Cord Inj Rehabil 2012;18(1):28–33
© 2012 Thomas Land Publishers, Inc.
Functional Electrical Stimulation in Spinal
Cord Injury: From Theory to Practice
Rebecca Martin, OTR/L, OTD,1 Cristina Sadowsky, MD,1,2
Kimberly Obst, OTR/L, MBA,1 Brooke Meyer, PT, DPT,1
and John McDonald, MD, PhD1,2
1The International Center for Spinal Cord Injury at Kennedy Krieger Institute, Baltimore, Maryland;
2Johns Hopkins School of Medicine, Baltimore, Maryland
This article outlines steps to practical application of functional electrical stimulation (FES) within activity-based restorative therapy
(ABRT). Drawing from current evidence, specific applications of FES intended to help restore function lost to spinal cord injury
and associated neurologic disease are discussed. The medical and therapeutic indications, precautions, and contraindications
are reviewed to help participants with appropriate patient selection, treatment planning, and assessment. Also included are
the physiological implications of FES and alterable parameters, including dosing and timing, for a desired response. Finally,
approaches to improve cortical representation and motor learning and to transition emerging movement into functional tasks are
reviewed. Key words: activity-based restorative therapy, functional electrical stimulation, spinal cord injury
application are well-documented in diagnoses
from knee osteoarthritis to stroke. Its use in spinal
cord injury (SCI), however, is only supported
by studies of small sample size, leading to what
amounts to insufficient evidence to determine
whether its use is clinically indicated and necessary.
Emerging research indicates that neural restoration
is possible; there is now a significant amount
of literature demonstrating the role of activity-
dependent neural plasticity in recovery of function
after SCI. Systematic application of FES in patients
with SCI provides a mechanism for optimizing the
neural activity amount below injury level, while
reducing secondary complications and improving
unctional electrical stimulation (FES)
has long been used in orthopedic and
neurological rehabilitation. Its efficacy and
The nervous system is capable of change in
response to stimulation. Permanent changes
are possible with long-term, repeated exposure.
The amount and type of activity plays a
critical role in both development and plasticity
within the nervous system, including gene
expression,1-5 modification of synaptic strength
(eg, LTP),6,7 synapse elimination,6 myelination
and maintenance of myelination,8-11 and axonal
growth.12-14 The widespread dependence of
development and plasticity in the central nervous
system (CNS) on neural activity suggests that
optimized neural activity might also be important
for regeneration, given the common cellular
mechanisms participating in development
and regeneration.8,15 There is further evidence
supporting this concept demonstrated by the
fact that increased and decreased neural activity
enhances and inhibits multiple components of
spontaneous regeneration, respectively.16-21
Clinically, a significant number of individuals
with so-called complete SCI retain some
connectivity across injury site; this could be
represented by nonfunctioning myelin or denuded
axons that could potentially provide conductivity
across injury site given optimal activation. In
patients with complete or incomplete SCI,
there is now proof of FES-induced activation of
the central pattern generator mechanism, and
increased stepping responses have been observed
in response to FES.22-24 Some patients who were
regularly treated with FES demonstrated improved
lower limb ASIA motor and sensory scores25 and
Functional Electrical Stimulation in SCI 29
decreased spasticity,26 indicating some degree of
neuromodulation and remediation of paralysis in
response to stimulation.
In addition to the incremental changes observed
in nervous system activity, overall health measures
demonstrate significant response to FES. If not
more important than the nervous system changes,
these benefits are more immediate and contribute
to significant quality of life improvements.
Cardiovascular conditioning can be achieved
and maintained in individuals with SCI following
FES training. FES exercise produced a 2-fold
increase in the oxygen uptake, a 3-fold increase in
ventilation rate, and a 5 beats per minute increase
in heart rate from the resting value in 7 volunteers
with C5 to T12 SCI.27 In another study, peak
oxygen uptake increased by 103% and maximum
power output increased by 113% after one year
of 3 times per week home-based FES ergometry
training in an individual with C6 motor complete
SCI.28 Similar results were found when training
2 to 3 times per week for 6 months at 30 or 50
rpm.29 Daily FES cycling for 4 weeks reversed the
femoral artery size reduction and decreased wall
compliance associated with SCI paralysis.30
Metabolic benefits have also been outlined,
including increases in lean muscle mass25 and
capillary number31 and decreases in adipose
tissue,32 in response to FES training. Beyond
body composition, FES has been demonstrated
to decrease blood glucose and insulin levels in
patients with SCI.25,33,34
The most well-studied aspect of FES training may
be the muscle and bone response. Muscles improve
in size, strength,35-37 and composition. Conversion
from type IIB to type IIA and type I muscle fibers
has been demonstrated,38 indicating improved
fatigue resistance and oxidative capacities.
Finally, FES leg cycle ergometer training results in
proportional increases in fiber area and capillary
Recovery of lost bone mass, demonstrated
especially in the lower extremities,40 is also
associated with FES. Improvements in muscle
mass and bone density may lead to fewer life-
threatening complications, including fractures,
pressure ulcers, and infections.
There are a wide variety of therapeutic
applications of FES. FES has been used to
maintain or increase range of motion, reduce
edema, promote healing of fracture or tissue,
reduce muscle spasm and the effects of spasticity,
improve circulation, prevent or reverse disuse
atrophy, and facilitate movement. It has also been
used for neuromuscular re-education and orthotic
substitution. Before moving too far into the
pragmatics of application, however, it is important
to note that there are 3 distinct types of electrical
stimulation commonly utilized in activity-based
1. Neuromuscular electrical stimulation
(NMES) is electricity applied across the
surface of the skin over an intact peripheral
nerve, which evokes an action potential in the
nerve fiber, causing an exchange of ions to
drive the muscle to contract. It includes FES.
2. Functional electrical stimulation (FES) is
the application of electrical stimulus to
a paralyzed nerve or muscle to restore or
achieve function. FES is most often used in
neurorehabilitation and is routinely paired
with task-specific practice. A common
example is orthotic substitution, also
known as a neuroprosthesis.
3. Transcutaneous electrical nerve stimulation
(TENS) is used for pain modulation by
exciting peripheral nerves using sensory,
motor, or noxious settings. Clinically,
TENS has been used for lower back pain,
neurogenic pain, arthritic pain, and various
other forms of pain. In activity-based
restorative therapy, TENS sensory settings
are also used to achieve sensory input to the
nervous system and for tone and spasticity
When applying any form of electrical
stimulation, it is important to keep in mind that
an electrically driven contraction differs from a
physiological contraction in 2 main ways. First, the
action potential (AP) generated in an electrically
30 Topics in spinal cord injury rehabiliTaTion/WinTer 2012
driven contraction travels both anterograde, to the
neuromuscular junction, and retrograde, to the
anterior horn cell. Second, the recruitment of motor
units differs in both type and number. Recruitment
of motor units by electrical stimulation progresses
from large to small, the reverse order of voluntary
contractions, because axons of the largest diameter
are the easiest to activate. Voluntary contractions
preferentially recruit force-producing, slow-
contracting, fatigue-resistant (type I) fibers,
before the more forceful, faster, fatigable (type
II) units. This allows for asynchronous activation
of varied motor units, which enables smooth
switching between active and inactive motor
units to maintain muscle activity, while allowing
recovery time for individual motor units and for
smooth and graded movement. Electrically elicited
contractions lack smooth, gradual onset, reflecting
biased and synchronous motor unit recruitment.
The contractions recruit motor units based on size
and proximity to the stimulation electrode. This
produces multiple combinations of motor units
that are activated, preventing graded and isolated
movement. This all or nothing recruitment is
also a factor in fatigue. Fatigue occurs more
rapidly in an electrically generated contraction,
as a greater portion of fatigable motor units is
necessary for a given contraction. Combining
voluntary contractions with ES produces the best
and strongest contraction, as ES recruits different
motor units that are not activated at a given
moment by a voluntary contraction.
It is important to critically evaluate a patient’s
medical history when determining whether he or
she is a candidate for treatment with FES. A history
of implanted electrical device, cancer, osteomyelitis,
thrombosis/hemorrhage, or epilepsy may exclude
a patient from treatment. Active metastases and
pregnancy may exclude a patient for a limited
time. In any case, it is incumbent on the treatment
team to evaluate the risks and benefits prior to
beginning treatment. More significant, when
deciding a course of treatment, it is important to
determine if the desired peripheral nerve is intact.
Lower motor neuron (LMN) syndrome results
from damage to axon or cell body in peripheral
nervous system. In SCI, this can occur with
damage to anterior horn cells, stretching of nerve
roots, foramenal stenosis or compression, cauda
equina/conus medularis injury, or associated
peripheral nerve injury (eg, brachial plexus). It is
characterized by the loss of voluntary movement,
low to no muscle tone, and absent reflexes. It
is commonly found at the level of injury or
with chronic injuries and comorbidities, like
impingement, stenosis, and traction neuropathies.
Upper motor neuron (UMN) syndrome results
from damage to the neural pathway above the
anterior horn (or the motor nuclei of cranial
nerves). It is characterized by decreased voluntary
movement, impaired or absent sensation, and
pathological reflexes. The easiest way to determine
LMN or UMN presentation is via reflexes. Intact
reflexes signal intact peripheral nerves or UMN
presentation, which would clear the way for FES
usage. However, due to long-term atrophy and
spotty innervations, these once intact reflexes
may be diminished. Therefore nerve and muscle
response to FES needs to be examined. Mulcahey,
Smith, and Betz showed that a muscle with intact
peripheral innervation should produce a grade 3
muscle contraction when stimulated at 10-20 Hz
and 200-400 μs.41 Their work specifically looked at
patterns of innervation in high tetraplegia, as an
indicator of FES application alone versus the use of
FES prior to the following muscle transfer. It is still
worth considering FES with an LMN patient, as
the results are unclear. Kern et al found that home-
based FES of denervated muscle resulted in rescue
of muscle mass and tetanic contractility in a 2-year
longitudinal prospective study of 25 patients
with complete conus/cauda equina lesions. They
also found important immediate benefits for the
patients, including improved cosmetic appearance
of lower extremities and the enhanced cushioning
effect for seating.42
Once it has been decided that a patient is a
suitable candidate for FES, the therapist should
determine appropriate parameters to yield the
desired response. Basic parameters for any form
of NMES are waveforms, intensity or amplitude,
frequency, pulse width, reciprocation, ramp,
and duration. These combine to create electrical
current. The goal, when selecting parameters,
is to generate the lowest possible current,
while maintaining the desired response. This
Functional Electrical Stimulation in SCI 31
will protect against fatigue. Parameters can be
manipulated to produce a desired response or in
response to patient’s reaction. For example, if a
patient complains of an uncomfortable pulsing,
the frequency can be increased to smooth the
contraction. Additional considerations while
selecting parameters are outlined in Table 1.
After appropriate parameters have been defined,
the range of FES applications is limited only by
the therapist’s creativity. Using careful electrode
placement and a trigger to time stimulation, a
therapist can generate a reach and grasp pattern,
stepping pattern, or sequence muscles to help
a patient transition from supine to sitting. A
stimulated reach and grasp pattern may be used
to compliment a self-feeding goal. A therapist
may choose to use the stimulation to augment a
patient’s own emerging function; where timing or
strength is lacking, the FES can assist. The therapist
may choose to use FES as a method to provide
high-repetition practice for a patient with no
active movement. FES can be applied in isolation
or to multiple muscle groups. It can be used within
the movement of a piece of equipment, like the
Biodex or ergometer, or to move freely through
space. FES intervention is intended to complement
treatment goals, which should be functional and
patient-centered, as with any intervention.
Table 1. Considerations for appropriate parameter selection
Goal Frequency Pulse width Intensity Notes
Increase comfort Increase Decrease Decrease Can also try using larger
Decrease electrical bleed Increase or decrease Decrease Decrease Can also try using smaller
Minimize fatigue DecreaseDecrease Decrease Overall, aim to minimize current,
consider variable waveform
To improve quality of tetanyIncrease Increase or decrease Decrease Look for smooth fused
1. Ono T, Inokuchi K, Ogura A, Ikawa Y, Kudo Y,
Kawashima S. Activity-dependent expression of
parathyroid hormone-related protein (PTHrP) in rat
cerebellar granule neurons. Requirement of PTHrP for
the activity-dependent survival of granule neurons. J
Biol Chem. 1997;272:14404-14411.
2. Muslimov I, Banker G, Brosius J, Tiedge H. Activity-
dependent regulation of dendritic BC1 RNA
in hippocampal neurons in culture. J Cell Biol.
3. Sgambato V, Abo V, Rogard M, Besson M, Deniau J.
Effect of electrical stimulation of the cerebral cortex on
the expression of the Fos protein in the basal ganglia.
Neuroscience. 1997;81: 93-112.
4. Karlsson M, Hallbook F. Kainic acid, tetrodotoxin
and light modulate expression of brain-derived
neurotrophic factor in developing avian retinal
ganglion cells and their tectal target. Neuroscience.
5. Mingo N, Cottrell G, Zhang L, Wallace M, Burnham
W, Eubanks J. Kainic acid-induced generalized
seizures alter the regional hippocampal expression of
the rat m1 and m3 muscarinic acetylcholine receptor
genes. Epilepsy Res. 1997;29:71-79.
6. Zhou Q, Poo M. Reversal and consolidation of
activity-induced synaptic modifications. Trends
7. Daoudal G, Debanne D. Long-term plasticity of
intrinsic excitability: learning rules and mechanisms.
Learn Mem. 2003;10:456-465.
8. McDonald J, Becker D, Sadowsky C, Jane J, Conturo
T, Schultz L. Late recovery following spinal cord
injury. Case report and review of the literature. J
9. McDonald J. Repairing the damaged spinal cord:
from stem cells to activity-based restoration therapies.
Clin Neurosurg. 2004;51:207-227.
10. Becker D, Sadowsky C, McDonald J. Restoring
function after spinal cord injury. Neurologist.
32 Topics in spinal cord injury rehabiliTaTion/WinTer 2012
11. Wilson G, Chiu S. Potassium channel regulation
in Schwann cells during early developmental
myelinogenesis. J Neurosci. 1990;10:1615-1625.
12. Howe C. Depolarization of PC12 cells induces
neurite outgrowth and enhances nerve growth factor-
induced neurite outgrowth in rats. Neurosci Lett.
13. Cantallops I, Routtenberg A. Activity-dependent
regulation of axonal growth: posttranscriptional
control of the GAP-43 gene by the NMDA
receptor in developing hippocampus. J Neurobiol.
14. van Oyen A, van Pelt J. Activity-dependent neurite
outgrowth and neural network development. Prog
Brain Res. 1994;102:245-259.
15. Grill W, McDonald J, Peckham P, Heetderks W, Kocsis
J, Weinrich M. At the interface: convergence of neural
regeneration and neural prostheses for restoration of
function. J Rehabil Res Dev. 2001;38:633-639.
16. Perreau V, Adlard P, Anderson A, Cotman C.
Exercise-induced gene expression changes in the rat
spinal cord. Gene Expr. 2005;12:107-121.
17. Engesser-Cesar C, Anderson A, Basso D, Edgerton
V, Cotman C. Voluntary wheel running improves
recovery from a moderate spinal cord injury. J
18. Cotman C, Engesser-Cesar C. Exercise enhances
and protects brain function. Exerc Sport Sci Rev.
19. van Praag H, Shubert T, Zhao C, Gage F. Exercise
enhances learning and hippocampal neurogenesis in
aged mice. J Neurosci. 2005;25:8680-8685.
20. Rhodes J, van Praag H, Jeffrey S, et.al. Exercise
increases hippocampal neurogenesis to high levels
but does not improve spatial learning in mice bred for
increased voluntary wheel running. Behav Neurosci.
21. Kempermann G, van Praag H, Gage F. Activity-
dependent regulation of neuronal plasticity and self
repair. Prog Brain Res. 2000;127:35-48.
22. Querry R, Pacheco F, Annaswamy T, Goetz L,
Winchester P, Tansey K. Synchronous stimulation and
monitoring of soleus H reflex during robotic body
weight-supported ambulation in subjects with spinal
cord injury. J Rehabil Res Dev. 2008;45(1):175-186.
23. Behrman AL, Lawless-Dixon AR, Davis SB, et al.
Locomotor training progression and outcomes
after incomplete spinal cord injury. Phys Ther.
24. Harkema S, Gerasimenko Y, Hodes J, et al. Effect
of epidural stimulation of the lumbosacral spinal
cord on voluntary movement, standing, and assisted
stepping after motor complete paraplegia: a case
study. Lancet. www.thelancet.com. Published May 20,
25. Griffin L, Decker M, Hwang J, et al. Functional electrical
stimulation cycling improves body composition,
metabolic and neural factors in persons with spinal
cord injury. J Electromyogr Kinesiol. 2009;19:614-
26. van der Salm A, Veltink PH, Izerman MJ, Groothuis-
Oudshoorn KC, Nene AV, Hermens HJ. Comparison
of electric stimulation methods for reduction of triceps
surae spasticity in spinal cord injury. Arch Phys Med
27. Bhambhani Y, Tuchak C, Burnham R, Jeon J, Maikala
R. Quadriceps muscle deoxygenation during
functional electrical stimulation in adults with spinal
cord injury. Spinal Cord. 2000;38: 630-638.
28. Kakebeeke T, Hofer P, Frotzler A, Lechner H, Hunt
K, Perret C. Training and detraining of a tetraplegic
subject: high-volume FES cycle training. Am J Phys
Med Rehabil. 2008;87:56-64.
29. Fornusek C, Davis GM. Cardiovascular and
metabolic responses during functional electric
stimulation cycling at different cadences. Arch Phys
Med Rehabil. 2008;89:719-725.
30. De Groot P, Crozier J, Rakobowchuk M, Hopman M,
Macdonald M. Electrical stimulation alters FMD and
arterial compliance in extremely inactive legs. Med
Sci Sports Exerc. 2005;37(8):1356-1364.
31. Nash MS, Montalvo BM, Applegate B. Lower
extremity blood how and responses to occlusion
ischemia differ in exercise-trained and sedentary
tetraplegic persons. Arch Phys Med Rehabil.
32. Scremin A, Kurta L, Gentili A, et al. Increasing muscle
mass in spinal cord injured persons with a functional
electrical stimulation exercise program. Arch Phys
Med Rehabil. 1999;80:1531-1536.
33. Jeon J, Weiss C, Steadward R, et al. Improved
glucose tolerance and insulin sensitivity after electrical
stimulation-assisted cycling in people with spinal cord
injury. Spinal Cord. 2002;40:110-117.
34. Jeon J, Hettinga D, Steadward R, Wheeler G, Bell G,
Harber V. Reduced plasma glucose and leptin after
12 weeks of functional electrical stimulation–rowing
exercise training in spinal cord injury patients. Arch
Phys Med Rehabil. 2010;91:1957-1959.
35. Johnston T, Betz R, Smith B, et al. Implantable FES
system for upright mobility and bladder and bowel
function for individuals with spinal cord injury. Spinal
36. Field-Fote EC, Lindley SD, Sherman AL. Locomotor
training approaches for individuals with spinal
cord injury: a preliminary report of walking-related
outcomes. J Neurol Phys Ther. 2005;29(3):127-137.
37. Postans NJ, Hasler JP, Granat MH, Maxwell DJ.
Functional electric stimulation to augment partial
weightbearing supported treadmill training for
patients with acute incomplete spinal cord injury: a
pilot study. Arch Phys Med Rehabil. 2004;85:604-
38. Davis G, Hamzaid N, Fornusek C. Cardiorespiratory,
metabolic, and biomechanical responses during
functional electrical stimulation leg exercise:
health and fitness benefits. Artificial Organs.
39. Chilibeck P, Jeon J, Weiss C, Bell G, Burnham R.
Histochemical changes in muscle of individuals
with spinal cord injury following functional
electrical stimulated exercise training. Spinal Cord.
40. Frotzler A, Coupaud S, Perret C, Kakebeeke T, Hunt
K, Eser P. Effect of detraining on bone and muscle
tissue in subjects with chronic spinal cord injury after
Functional Electrical Stimulation in SCI 33 Download full-text
42. Kern H, Carraro U, Adami N, et al. Home-based
functional electrical stimulation rescues permanently
denervated muscles in paraplegic patients with
complete lower motor neuron lesion. Neurorehabil
Neural Repair. 2010;24:709.
a period of electrically-stimulated cycling: a small
cohort study. J Rehabil Med. 2009;41:282-285.
41. Mulcahey M, Smith B, Betz R. Evaluation of the
lower motor neuron integrity of upper extremity
muscles in high level spinal cord injury. Spinal Cord.